Endocrinology Flashcards
1
Q
Viruses that can trigger T1DM
A
Coxsackie B virus
Enterovirus
2
Q
Ideal blood glucose concentration
A
4.4-6.1mmol/L
3
Q
T1DM presentation
A
Polyuria Polydypsia Weight loss Secondary enuresis Recurrent infections Symptoms present 1-6weeks before developing DKA
4
Q
Bloods for T1DM
A
FBC, UE
Blood culture if fever
HbA1c
TFT, TPO to test for autoimmune thyroid disease
Anti-TTG for coeliac disease
Insulin antibodies, anti-GAD antibodies, islet cell antibodies
5
Q
Management of T1DM
A
Subcutaneous insulin regimes
Monitoring dietary carbohydrate intake
Monitoring blood sugar levels on waking, at each meal and before bed
Monitoring for and managing complications, both short and long term
6
Q
Insulin in T1DM
A
Background, long acting insulin given once a day
Short acting insulin given 30minutes before meals
Insulin pump
Cycle injection sites
7
Q
Insulin pump
A
Cannula pumps insulin into body
Replaced ever 2-3 days
To qualify: >12 and difficulty controlling HbA1c
8
Q
Advantages of insulin pump
A
Better blood sugar control
More flexibility in eating
Fewer injections
9
Q
Disadvantages of an insulin pump
A
Learning how to use pump
Having it attached at all times
Blockages in infusion set
Small risk of infection
10
Q
Types of insulin pumps
A
Tethered pump
Patch pump
11
Q
Tethered pumps
A
Replaceable infusion sets and insulin
Attached to patients belt or around waist
Controls on pump
12
Q
Patch pumps
A
Sit directly on skin without visible tubes
Entire patch has to be replaced
Controlled by separate remote
13
Q
T1DM hypoglycaemia causes
A
Too much insulin Not enough carbohydrates Not processing carbohydrates properly Malabsorption Diarrhoea Vomiting Sepsis
14
Q
Hypoglycaemia symptoms
A
Tremor Sweating Irritability Dizziness Pallor
Reduced consciousness
Coma and death
15
Q
Management of mild hypoglycaemia
A
Rapid acting glucose
Slower acting carbohydrates
16
Q
Management of severe hypoglycaemia
A
IV 10% dextrose:
2mg/kg bolus
5mg/kg bolus
IM glucagon
17
Q
Causes of hypoglycaemia
A
Hypothyroidism Glycogen storage disorders Growth hormone deficiency Liver cirrhosis Alcohol and fatty oxidation defects
18
Q
Nocturnal hypoglycaemia
A
Sweating overnight
19
Q
Long term macrovascular complications of hyperglycaemia
A
Coronary artery disease
Peripheral Ischaemia: poor healing, ulcers, diabetic foot
Stroke
Hypertension
20
Q
Long term microvascular complications of hyperglycaemia
A
Peripheral neuropathy
Retinopathy
Kidney disease, glomerulosclerosis
21
Q
Infection-related complications of hyperglycaemia
A
UTI
Pneumonia
Skin and soft tissue infections, especially in the feet
Fungal infections, especially oral and vaginal candidiasis
22
Q
T1DM monitoring
A
HbA1c every 3-6 months
Capillary blood glucose
Flash glucose monitoring: Libre, checks glucose in interstitial fluid, 5 minute lag behind blood glucose. Need replacing every 2 weeks
23
Q
T2DM in children
A
Increased body weight Increased risk of renal complications HTN Dyslipidaemia Increased cardiovascular risk
24
Q
T2DM treatment
A
Lifestyle modification
Paediatric dietician to optimise body-weight and blood glucose control
Anti diabetic drugs
>6 months influenza and pneumococcal immunisation
Target HbA1c: 48mmol.mol
25
Anti diabetic drugs in children
Only Metformin hydrochloride
Increase dose gradually
3-4 months
If not working, add long acting insulin or once-daily human isophane insulin
26
DKA main problems
Ketoacidosis
Dehydration
Potassium imbalance
27
Potassium imbalance DKA
```
No insulin to drive potassium into cells
Serum K high, total K low
Kidneys remove K as serum K is high
Add insulin, hypokalaemia, low serum potassium
Arrhythmias
```
28
Cerebral oedema DKA
```
Dehydration, high blood sugar
Water moves ICF-> ECF in brain
Brain cells shrink and become dehydrated
Rapid correction of dehydration and hyperglycaemia
ECF-> ICF
Brain swells and becomes oedematous
Brain cell destruction and death
```
29
Signs of cerebral oedema
Headaches
Altered behaviour
Bradycardia
Changes to consciousness
30
Management for cerebral oedema
Slowing IV fluids
IV mannitol
IV hypertonic saline
31
Presentation of DKA
```
Hyperglycaemia, dehydration, acidosis
Polyuria
Polydipsia
N/V
Weight loss
Acetone smell to breath
Dehydration and subsequent hypotension
Altered consciousness
Symptoms of underlying trigger (sepsis)
```
32
DKA diagnosis
Blood glucose >11
Ketosis >3 mmol/l
Acidosis pH<7.3
33
Principles of DKA management in children
```
Correct dehydration over 48 hours
Fixed rate insulin infusion
Avoid fluid boluses
Treat underlying triggers
Prevent hypoglycaemia: IV dextrose once blood glucose falls <14mmol/L
Add potassium to IV fluids and monitor serum potassium closely
Monitor for signs of cerebral oedema
Monitor glucose, ketones and pH
```
34
Addison’s disease
Adrenal glands damaged
Reduced cortisol and aldosterone secretion
Primary adrenal insufficiency
Autoimmune cause
35
Secondary adrenal insufficiency
Inadequate ACTH stimulating adrenal glands
Low levels of cortisol released
Congenital underdevelopment of pituitary gland
Pituitary Hypoplasia, surgery, infection, loss of blood flow, radiotherapy
36
Tertiary adrenal insufficiency
Inadequate CRH released by hypothalamus
| Long term oral steroids (>3 weeks) causing suppression of hypothalamus
37
Features of adrenal insufficiency in babies
```
Lethargy
Vomiting
Poor feeding
Hypoglycaemia
Jaundice
Failure to thrive
```
38
Features of adrenal insufficiency in older children
N/V
Poor weight gain or weight loss
Reduced appetite (anorexia)
Abdominal pain
Muscle weakness or cramps
Developmental delay or poor academic performance
Bronze hyperpigmentation to skin in Addisons: high ACTH levels which stimulate melanocytes
39
Adrenal insufficiency investigations
UE: hyponatraemia, hyperkalaemia, hypoglycaemia
| Test for cortisol, ACTH, aldosterone and renin levels
40
Addison’s disease hormone levels
Low cortisol
High ACTH
Low aldosterone
High renin
41
Secondary adrenal insufficiency
Low cortisol
Low ACTH
Normal aldosterone
Normal renin
42
Short synacthen test
| ACTH stimulation test
Performed in morning when adrenal glands are most fresh
Test involves giving synacthen
Blood cortisol measured at baseline, 30 and 60 minutes after administration
Cortisol level should at least be double in response to synacthen
43
Management of adrenal insufficiency
Replacement steroids
Hydrocortisone for cortisol (glucocorticoid)
Fludrocortisone for aldosterone (mineralocorticoid)
Steroid card and emergency ID tag
Increases doses in acute illness
44
Monitoring of adrenal insufficiency
```
Growth and development
Blood pressure
U&Es
Glucose
Bone profile
VitaminD
```
45
During acute illness (sick day rules)
>38degrees temperature
Vomiting and diarrhoea
Dose of steroid increased and given more regularly
Blood sugar needs to be monitored closely
Need to eat food containing carbohydrates regularly
D/V, need IM injection of steroid at home and likely required admission for IV steroids
46
Addisonian crisis
Acute presentation of severe Addisons
Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia
47
Management of Addisonian crisis
```
Intensive monitoring
Parenteral steroids
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance
```
48
Polydipsia in children
Central diabetes insipidus
Nephrogenic diabetes insipidus
Diabetes mellitus TY1
Diabetes mellitus TY2
49
Puberty in males
First sign: testicular growth at 12 years
Testicular volume >4ml indicates onset of puberty
Maximum height spurt at 14
50
Puberty in females
First sign is breast development at 11.5 years of age
Height spurt reaches maximum at 12, before menarche
Menarche at 13
51
Normal changes in puberty
Gynaecomastia may develop in boys
Asymmetrical breast growth may occur in girls
Diffuse enlargement of the thyroid gland may be seen
52
Delayed puberty with short stature
Turner’s syndrome
Prader-Willi syndrome
Noonan syndrome
53
Delayed puberty with normal stature
Polycystic ovarian syndrome
Androgen insensitivity
Kallman’s syndrome
Klinefelter’s syndrome
54
Precocious puberty
Development of secondary sexual characteristics before 8 years in females and 9 years in males
More common in females
Gonadotropin dependent, gonadotropin independent
55
Gonadotropin dependent precocious puberty
Due to premature activation of HPA axis
| FSH/LH raised
56
Gonadotropin independent precocious puberty
Due to excess sex hormones
| FSH/ LH low
57
Testes precocious puberty
Bilateral enlargement= gonadotropin release from intracranial lesion
Unilateral enlargement- gonadal tumour
Small tests: adrenal cause, tumour or adrenal hyperplasia
58
Organic causes of precocious puberty in females
Usually idiopathic or familial and follows normal sequence of puberty
Organic cases are rare
McCune Albright syndrome
59
Congenital adrenal hyperplasia
Congenital deficiency of 21-hydroxylase enzyme
Underproduction of cortisol and aldosterone
Over production of androgens from birth
Autosomal recessive inheritance
60
Testosterone function
Androgen hormone
High levels in men
Low levels in women
Promotes male sexual characteristics
61
Glucocorticoids function
Deal with stress, raise blood glucose, reduce inflammation, suppress immune system
Cortisol: main glucocorticoid hormone
Level of cortisol fluctuates during the day, higher levels in morning and during times of stress
Released in response to ACTH from anterior pituitary
62
Mineralocorticoid hormones
Act on kidneys to control balance of salt and water in blood
Aldosterone secreted by adrenals in response to renin
Acts on kidneys to increase sodium reabsorption into blood and increase potassium secretion into urine
Aldosterone acts to increase sodium and decrease potassium in the blood
63
Pathophysiology congenital adrenal hyperplasia
21-hydroxylase Converts progesterone into aldosterone and cortisol
21-hydroxylase deficiency
Excess progesterone -> testosterone
64
Presentations in severe cases of CAH
Virilised genitalia: ambiguous genitalia and an enlarged clitoris due to the high testosterone levels
Severe CAH: hyponatraemia, hyperkalaemia, hypoglycaemia
Poor feeding
Vomiting
Dehydration
Arrhythmias
65
Female patients mild CAH
```
Tall for their age
Facial hair
Absent periods
Deep voice
Early puberty
```
66
Male patients with mild CAH
```
Tall for their age
Deep voice
Large penis
Small testicles
Early puberty
```
67
Management of CAH
Cortisol replacement with hydrocortisone
Aldosterone replacement, fludrocortisone
Virilised genitals: corrective surgery
68
Congenital growth hormone deficiency
Disruption to growth hormone axis at hypothalamus or pituitary gland
GH1 or GHRHR mutation
Empty sella syndrome: pituitary gland is underdeveloped or damaged
69
Acquired growth hormone deficiency
Secondary to infection, trauma, surgical interventions
70
Multiple pituitary hormone deficiency
```
Hypopituitarism
Hypothyroidism
Growth hormone deficiency
Adrenal insufficiency
Gonadotropin
```
71
Presentation of GH deficiency in neonates
Micro penis
Hypoglycaemia
Severe jaundice
72
Presentation of GH deficiency in older infants and children
Poor growth, usually stopping or severely slowing from age 2-3
Short stature
Slow development of movement and strength
Delayed puberty
73
GH deficiency investigations
GH stimulation test: use glucagon, insulin, arginine or clonidine
Thyroid and adrenal deficiency
MRI brain for pituitary or hypothalamus abnormalities
Genetic testing for Turner, Prader-Willi
X-RAY or DEXA scan to determine bone age and help predict final height
74
Treatment of GH deficiency
Daily s.c. Somatropin (GH)
Treatment of other associated hormone deficiencies
Close monitoring of height and development
75
Congenital hypothyroidism
Dysgenesis or dyshormonogenesis
| Newborn blood spot screening test
76
Congenital hypothyroidism presentation
```
Prolonged neonatal jaundice
Poor feeding
Constipation
Increased sleeping
Reduced activity
Slow growth and development
```
77
Acquired hypothyroidism causes
Autoimmune thyroiditis (Hashimotos)
TY1DM and coeliac associations
Anti thyroid peroxidase antibodies and anti thyroglobulin antibodies
78
Symptoms of acquired hypothyroidism
```
Fatigue and low energy
Poor growth
Weight gain
Poor school performance
Constipation
Dry skin and hair loss
```
79
Management of hypothyroidism
TFTs
Thyroid ultrasound
Thyroid antibodies
Levothyroxine O.D.
80
Thyrotoxicosis in pregnancy
Increase in TBG, increase in levels of total thyroxine but doesn’t affect free thyroxine level
Untreated thyrotoxicosis increases risk of foetal loss, maternal heart failure and premature labour
Graves most common cause
HCG can activate TSH receptor: transient gestational hyperthyroidism
81
Management of hyperthyroidism in pregnancy
First trimester: propylthiouracil
Second trimester: carbimazole
T3/4 levels checked, don’t want hypothyroidism in fetus
TSH-receptor simulating antibodies check at 30-36 weeks
82
What BMI centile would you consider tailored clinical intervention for obesity?
>91st
83
When BMI centile would you consider assessing for obesity comorbidities?
>98th centile
84
Risk factors for obesity in children
Asian children
Female children
Taller children: >50th percentile in height
85
Cause of obesity in children
```
GH deficiency
Hypothyroidism
Down’s syndrome
Cushing’s syndrome
Prader-Willi syndrome
```
86
Consequences of obesity in children
Orthopaedic problems: SUFE, Blount’s disease, MSK pains
Psychological consequences: poor self-esteem, bullying sleep apnoea
Benign intracranial HTN
TY2DM
HTN
Ischaemic heart disease
